The current status of nucleotide excision repair in the yeast \u3ci\u3eSaccharomyces cerevisiae\u3c/i\u3e

The removal of UV radiation-induced pyrimidine dimers and (6–4) photoproducts as well as other bulky base adducts from the DNA of higher eukaryotes relies on the concerted action of about 30 proteins which excise base damage and restore the DNA to its native state. This process is known as nucleotide excision repair (NER), and the proteins involved are highly conserved throughout the eukaryotae. There are indications that the initial steps of NER are effected by a large performed multi-protein complex comprising the RNA polymerase II transcription factor IIH (TFIIH) and other NER proteins known to be required for damage recognition and DNA incision. Humans with inactivating mutations in the genes encoding NER proteins suffer from the cancer-prone syndrome xeroderma pigmentosum (XP). In yeast, a mode of NER which is apparently coupled to transcription requires the activity of Rad26 protein, while transcription-independent NER requires the activity of the Rad7 and Rad16 proteins. Defects in transcription-dependent NER are associated with the human hereditary disorder Cockayne syndrome (CS)